a-catenin is a unique protein with a dual role; it functions as both a key cytoskeletal component and as an important messenger in the Wnt signaling cascade. Beta-catenin has been implicated in numerous processes in normal development, carcinogenesis and disease. Previous work by our lab and others has shown that beta-catenin plays an important role in the development of the mouse neocortex. We propose to further the understanding of beta-catenin's role in the embryonic cortex using loss of function experiments designed to address the following questions: (1) Will the loss of beta-catenin change the fraction of neural precursor cells that exit the cell cycle? (2) What are the relative contributions of beta-catenin adhesion and signaling in neural precursors? We plan to answer these questions using a novel approach in which beta- catenin is deleted from only a small fraction of neural precursor cells. This will allow us to study precursor cells lacking beta-catenin in the context of a wild-type cortex, enabling us to draw conclusions about the cell- autonomous effects of the loss of beta-catenin.